Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.01 seconds)

Liver plasma membranes (LPM) were isolated from rats fed an essential fatty acid-supplemented diet (+EFA) or from rats fed an essential fatty acid-deficient diet (-EFA). The proportions of linoleate and arachidonate in membrane total fatty acids in the -EFA preparations were one-half or less than the values for the +EFA preparations. Basal, F-, or glucagon-stimulated adenylate cyclase activities were significantly lower in EFA-deficient livers than in nondeficient ones. Addition of GTP significantly enhanced glucagon-stimulated adrenylate cyclase in both groups, but extent of stimulation above basal was greater in EFA-deficient livers. Portal vein injection of glucagon in vivo resulted in significantly higher cAMP formation in +EFA livers than in -EFA livers. When glucagon was used in vitro at 1-1,000 nM, stimulation of adenylate cyclase remained lower in EFA-deficient membranes, but extent of stimulation above basal activity was larger in -EFA membranes than in +EFA. Total Na+, K+ (Mg2+)-ATPase from EFA-depleted LPM exhibited significantly higher values of apparent Km and Vmax-5'-Nucleotidase activity, in contrast, was considerably decreased in EFA-deficient rats. These findings show that, in animals, changes in unsaturated fatty acid composition can affect the properties of membrane-bound enzymes. These alterations could be due to changes in membrane physical properties and/or prostaglandin formation.
 ...
PMID:Effect of essential fatty acid deficiency on activity of liver plasma membrane enzymes in the rat. 18 Mar 55

The results of clinical and biochemical investigations on a girl with all obligatory signs of Mauriac syndrome already in infancy were compared with the different hypotheses suggested in order to explain the pathogenesis of this disease. One possible explanation for the origin of MS might be a decreased sensitivity of adenylate-cyclase to glucagon or adrenalin. Hypersensitivity to insulin, resulting in a decreased production of cyclic AMP and activation of glycogen synthetase could be excluded by measuring the urine excretion of cAMP with and without insulin. Furthermore no signs of dyspituarism were detectable on our case and the hypothesis of MS being a combination of primary glycogenosis and diabetes mellitus could also be refuted. Liver enzyme activities were normal.
 ...
PMID:[Pathogenetic investigations on a case of mauriac syndrome (author's transl)]. 18 11

Glucagon causes a rapid activation of cAMP-dependent protein kinase in rat liver parenchymal cells which correlates well with the accumulation of cAMP. Full activation of phosphorylase or inactivation of glycogen synthase is achieved with half-maximal or less activation of protein kinase. Epinephrine stimulates glycogen breakdown in these cells mainly by mechanisms involving alpha-adrenergic receptors and not beta-receptors. Activition of alpha-receptors results in rapid activation of phosphorylase and inactivation of glycogen synthase without accumulation of cAMP or activation of cAMP-dependent protein kinase. Activation of beta-receptors causes a transient rise in cAMP and a short-lived activation of protein kinase with correspondingly little stimulation of glycogenolysis.
 ...
PMID:Studies on the role of cAMP-dependent protein kinase in the actions of glucagon and catecholamines on liver glycogen metabolism. 18 93

Insulin release in the perfused isolated rat pancreas was measured after stimulation with 16.5 mM glucose with and without somatostatin (cycle form, 100 ng/ml) in the medium. A complete blockage of the typical biphasic pattern of insulin release ocurred with somatostatin in the medium. Such blockage was abolished when cAMP (2.5 mM) and a 0.5 ml solution of glucagon (1 mg/ml) were continuously perfused for 20-minute periods and for 30-second periods correspondently. It did not take place when glibenclamide (HB-419) was perfused for a 20-minute period at a rate of 10 mug/ml. The results suggest that the adenylcyclase dependent mechanisms of glucose-induced insulin release are involved in the inhibition of the glucose-induced insulin secretion by somatostatin.
 ...
PMID:Inhibition of the glucose induced insulin release by somatostatin in the isolated perfused rat pancreas. Action of cyclic AMP, glucagon and glibenclamide. 18 68

Infusion of 2 MRC/kg X h calcitonin in anaesthetised dogs produced a significant increase in plasma-renin activity, clearance of 51Dr-EDTA and 125I-o-iodohipuric acid, heart rate and urinary excretion of sodium, potassium, calcium and phosphates, while serum electrolytes and mean arterial pressure markedly fell. Infusion of 5 mug/kg X min glucagon produced a significant fall of plasma-renin, heart rate rose, but arterial mean pressure fell, and serum and urinary electrolytes did not change significantly, Cyclic AMP (dibutyryl-cAMP) significantly stimulated renin at a dose of 5 mg/min, while there were no significant changes in blood pressure, heart rate and serum and urinary electrolytes.
 ...
PMID:[The effects of calcitonin, glucagon and the dibutyryl derivative of cyclic AMP on plasma-renin activity (author's transl)]. 18 47

The concentration of insulin and glucagon in peripheral blood and the concentration of cAMP in liver was followed in rats throughout a 48 hour starvation period and up to 6 hours afer refeeding glucose or casein. By so changing the insulin/glucagon molar ratio from minimum to maximum values, simultaneous inverse changes in the concentration of hepatic cAMP could be induced. The study, thus, suggests that during a starvation-refeeding cycle the level of cAMP in the liver is regulated predominantly by the insulin/glucagon ratio in the blood. Possible criticisms of this conclusion are discussed.
 ...
PMID:Concentration of cyclic AMP in rat liver as a function of the insulin/glucagon ratio in blood under standardized physiological conditions. 18 53

The glucagon and insulin release induced by amino acids was studied in the presence of glucose, dibutyryl cyclic AMP (dbcAMP) or theophylline on the splenic part of the pancreas of new born rats (48 to 64 hours). The results were compared to the literature data. Arginine or a mixture of the three amino acids (A.A.), arginine, lysine or alanine, stimulate glucagon secretion at 1.6 mM glucose. This stimulation is suppressed by 16.7 mM glucose. On the other hand, 16.7 mM glucose potentiates the effect of arginine or of the 3 A.A. on insulin release. At 1.6 mM glucose, theophylline potentiates the effect of 3 A.A. (10 mM each) on glucagon and insulin release : this effect reaches a maximum at 5 mM of theophylline; dbcAMP also potentiates the effect of 3 A.A. on glucagon and insulin release, and the effect of arginine, alanine or lysine on glucagon release. On the beta cell, the lack of potentiation observed between dbcAMP and arginine, lysine or alanine indicates that these A.A. interact positively when mixed together. In the presence of arginine or of the three A.A., the percentage stimulation of glucagon and insulin release depends on the dbcAMP dose and does not vary with the glucose concentration. The increase of glucagon and insulin release observed when the NaCl concentration in the incubation medium decreases cannot account for our results. Cyclic GMP (4 mM) does not modify the glucagon or insulin secretion induced by different concentrations of glucose or by the mixture of A.A. (10 mM each). The stimulating effect of acetylcholine on insulin release would not be related to the cyclic GMP molecule. In conclusion, instead of modifying the specificity of substrate, theophylline or dbcAMP accentuate it: glucose stimulates specifically the beta cell whereas 3 A.A. are more effective on the alpha2 cell than the beta cell. Cyclic AMP suppresses the glucose effect on glucagon release induced by the amino acids. Because of its interaction with glucose and amino acids, cyclic AMP seems to be a very important element in the regulation of the release of these pancreatic hormones.
 ...
PMID:Regulation by glucose and cyclic nucleotides of the glucagon and insulin release induced by amino acids. 18 41

The physiologic significance of glucocorticoids and insulin in the regulation of hepatic gluconeogenesis was investigated during a 48-hr starvation period by studying the factors presumed to control the rate of glucose synthesis in the final gluconeogenetic pathway. Rats were used, in which glucorticoids were removed by adrenalectomy before starvation, and in which serum insulin was kept constant before and after food withdrawal by pre-feeding with a proteinfree diet. It was found that adrenalectomized rats at constantly low serum insulin levels responded to starvation as rapidly, and to the same degree, as intact control subjects (1) by a significant increase in plasma glucagon and, consequently, in hepatic cAMP concentration; (2) by a coordinate elevation of the activities of hepatic pyruvate carboxylase, P-enolpyruvate carboxykinase, and fructose-1,6-diphosphatase; (3) by systematic alterations in the concentration of effectors of gluconeogenetic key enzymes; (4) by a shifting of the cytoplasmic NAD system towards the reduced state; (5) by a decrease in the intrahepatic concentration of glycogenic precursor substrates. These results suggest that the hepatic gluconeogenic response to starvation with respect to the regulatory factors 1-5 occurs independently from changes in the concentration of plasma glucocorticoids and insulin. The crossing over of the gluconeogenetic intermediates between pyruvate and P-enolpyruvate (PEP), which was observed in intact but not in adrenalectomized rats, supports the assumption that during starvation, glucocorticoids enhance the rate of glucose production by the liver predominantly by permitting hepatic cAMP to stimulate the yet undefined mechanism, which has been demonstrated in the isolated perfused rat liver to control the substrate flow between pyruvate and PEP.
 ...
PMID:Physiologic significance of glucocorticoids and insulin in the regulation of hepatic gluconeogenesis during starvation in rats. 18 90

There is evidence than adenosine 3',5'-monophosphate (cAMP) and guanosine 3',5'-monophosphate (cGMP) may have antagonistic actions on cell growth, with cAMP inhibiting and cGMP stimulating this process. However, reductions in cAMP and increases in cGMP are not charactersitic of all neoplastic tissues. Thus, benign and malignant tissues from hepatoma-bearing rats exposed to the hepatic carcinogen DL-ethionine have elevated rather than depressed cAMP, compared to control liver, and parenteral administration of this drug increases hepatic cAMP within hours. In the present study, the effects of ethionine ingestion on the hepatic content and metabolism of both cAMP and cGMP were examined sequentially in rats at 2 and then 6 wk intervals, from the initiation of drug administration until the development of hepatomas. After 2 wk, cAMP content of quick-frozen liver from rats receiving ethionine (E) was significantly increased (826 +/- 91 pmole/g wet weight) above that of liver from pair-fed controls (C, 415 +/- 44), whether calculated by tissue wet weight, protein, or DNA content. In benign tissue from E, higher cAMP was still evident after in vitro incubations of slices with 2 mM 1-methyl-3-iso-butylxanthine (MIX) and was associated with enhanced adenylate cyclase and unchanged high or low Km cAMP-phosphodiesterase activities. These findings are compatible with accelerated cAMP generation in liver from E. Protein kinase activity ratios were significantly increased in frozen liver from E (0.52 +/- 0.04 versus 0.36 +/- 0.03 in C), and the percent glycogen synthetase in the I form was clearly reduced (19% +/- 2% in E versus 47% +/- 5% in c). incubation of hepatic slices from E or C with MIX and/or 10 muM glucagon further increased cAMP and protein kinase activity ratios, data which imply higher effective, as well as total, cellular cAMP in E. Changes in cAMP metabolism and action observed at 2 wk persisted throughout the 38-wk period of drug ingestion. Adenylate cyclase activity, cAMP content, and protein kinase activity ratios of ethionine-induced hepatomas exceeded those of both the surrounding liver from tumor-bearing rats and that of control liver, but alterations in these parameters were qualitatively similar in both tissues from E. By contrast, while cGMP in quick-frozen surrounding liver from tumor-bearing rats (36 +/- 4 pmole/g wet weight) did not differ from that of control liver (30 +/- 3), cGMP in the hepatomas was increased. This change was evident in both frozen tumor (89 +/- 10) and in tumor slices incubated in vitro with MIX (C, 90 +/- 11; surrounding liver, 85 +/- 10; hepatoma 231 +/- 29). These results indicate that malignant conversion can occur in liver with a sustained elevation of both total and effective cAMP during the premalignant phase. The increase in cGMP detected in ethionine-induced hepatomas could also be a key determinant of malignant transformation in the model, although premalignant changes in cGMP were not apparent.
 ...
PMID:Sequential alterations in the hepatic content and metabolism of cyclic AMP and cyclic GMP induced by DL-ethionine: evidence for malignant transformation of liver with a sustained increase in cyclic AMP. 18 92

Fat cells were preincubated for 2 h in the presence and absence of growth hormone (GH) and Dexamethasone (Dex) before the addition of increasing concentrations of either epinephrine, theophylline or glucagon and final incubation of the cells for an additional 5 minutes. GH and Dex increased by 85%, 28% and 72%, respectively, the cAMP levels reached in the sole presence of 10(-5)M epinephrine, 10(-2)M theophylline or 5 X 10(-5)M glucagon. An adenylate cyclase particulate preparation shows that epinephrine decreases Km from 2mM to 0.6 MM and increases Vmax and the strength of interaction value (n) from 0.91 to 1.75.
 ...
PMID:Hormonal control of fat cells adenylate cyclase. 18 30


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>